The article discusses the cellular and molecular mechanisms of ionizing radiation-induced oxidative stress and its prolonged effects on cells. Ionizing radiation can directly disrupt atomic structures and indirectly generate reactive oxygen and nitrogen species (ROS and RNS) through water radiolysis. These reactive species can damage DNA, proteins, and lipids, leading to cellular dysfunction and death. The oxidative stress caused by radiation can spread from targeted cells to non-targeted bystander cells through intercellular communication mechanisms, affecting their oxidative metabolism and leading to long-term health risks, including genomic instability and neoplastic transformation. The article also highlights the role of mitochondria in mediating delayed effects of ionizing radiation, such as mitochondrial DNA damage, protein import defects, and changes in metabolic enzymes. The persistence of these oxidative stress-induced changes in progeny cells has significant implications for health risks, including neurodegeneration, cardiovascular diseases, and cancer. Understanding the molecular and biochemical events that promote early and late oxidative stress in irradiated cells is crucial for developing strategies to counteract adverse health effects of ionizing radiation.The article discusses the cellular and molecular mechanisms of ionizing radiation-induced oxidative stress and its prolonged effects on cells. Ionizing radiation can directly disrupt atomic structures and indirectly generate reactive oxygen and nitrogen species (ROS and RNS) through water radiolysis. These reactive species can damage DNA, proteins, and lipids, leading to cellular dysfunction and death. The oxidative stress caused by radiation can spread from targeted cells to non-targeted bystander cells through intercellular communication mechanisms, affecting their oxidative metabolism and leading to long-term health risks, including genomic instability and neoplastic transformation. The article also highlights the role of mitochondria in mediating delayed effects of ionizing radiation, such as mitochondrial DNA damage, protein import defects, and changes in metabolic enzymes. The persistence of these oxidative stress-induced changes in progeny cells has significant implications for health risks, including neurodegeneration, cardiovascular diseases, and cancer. Understanding the molecular and biochemical events that promote early and late oxidative stress in irradiated cells is crucial for developing strategies to counteract adverse health effects of ionizing radiation.